Abstract Book

S1269

ESTRO 37

controlled studies. However, adjacent anatomic structures of the prostate limit the use of high-doses. Our aim was to evaluate the relationship between TCP (Tumor Control Probability) and NTCP (Normal Tissue Complication Probability) in patient who were treated with HdRT. Material and Methods Twenty patients who were treated with HdRT for low-risk PC between January 2015 and November 2015 were included. Simulation was performed with a full bladder and empty rectum. The entire bladder and rectum were contoured as normal tissues. PTV was generated with 1cm margins in all directions (except posteriorly 0.7 cm) from the prostate. The total prescription dose for all patients was 78 Gy with VMAT technique. The TCP, NTCP rectum , NTCP bladder data were calculated using the Lyman/Rancati model in the Eclipse® planning system. The TCP, NTCP bladder and NTCP rectum for each ±1% dose change (± 1-5%) at the target were performed. Statistical analysis was calculated using the Spearman test. Results The median prostate PTV, rectum and bladder volumes were 153 (82.8-108.9), 56 (32.5-121.2), 143.8 (72.6- 533.2) cm 3 and the median TCP, NTCP rectum, NTCP bladder for PTV 78 Gy were 98%(97.4-98.3), 3.4%(0.9-6.1), 53.2%(6.4- 81.4) respectively. Reduction of the dose by 1% the TCP, NTCP rectum, NTCP bladder changed 0.5%(0.4-0.6), 4.1%(1.1- 4.5), 0.3%(0.1-0.5) for 1%; 1%(0.9-1.2), 8.2%(2.0-9.0), 0.5%(0.1-0.9) for 2%; 1.6%(1.4-2.0), 11.9%(2.8-13.5), 0.7%(0.2-1.3) for 3%; 2.4% (2.1-2.9), 15.9%(3.4-17.7), 1.0%(0.2-1.7) for 4%; and 3.3%(2.9-4.0), 19.9%(4.0-22.0), 1.1%(0.3-2.0) for 5% respectively. For 1% increase in doses the changes in percentage ratios for TCP, NTCP bladder , NTCP rectum were: 0.4%(0.2-0.4), 3.9%(1.3-4.7), 0.3%(0.1-0.6) for 1%; 0.7%(0.6-0.8), 7.7%(2.8-9.4), 0.7%(0.2-1.1) for 2%; 0.9%(0.8-1.2), 11.5%(4.6-14.0), 1.0%(0.3-1.8) for 3%; 1.1%(1.0-1.4), 15.3%(6.6-18.5), 1.4%(0.4-2.5) for 4% and 1.3%(1.1-1.7), 19.5%(9.0-23.2), 1.9%(0.5-3.2) for 5% respectively. In the case of 5% dose reduction at the target, TCP decreased by 2.8%, whereas 15.8% was gained in NTCP bladder and 0.8% was gained in NTCP rectum . With a dose increase of 5%, 0.9% was gained in TCP and 15% was gained in NTCP bladder whereas a loss of 1.6% occurred in NTCP rectum . However, we were unable to demonstrate a statistically significant correlation between TCP and NTCP depending on dose changes due to the limited number of patients. Conclusion The calculation models based on biological fundaments as well as the normal tissue tolerance limits should also be taken into consideration by increasing the dose to the target volume. EP-2300 TCP modelling of a hypoxic subvolume within the prostate. T.J. McMullan 1 , D.B. McLaren 2 , W.H. Nailon 1 1 Edinburgh Cancer Centre, Oncology Physics, Edinburgh, United Kingdom 2 Edinburgh Cancer Centre, Clinical Oncology, Edinburgh, United Kingdom Purpose or Objective Tumour hypoxia is a common feature in prostate cancer, and is associated with radiotherapy failure. A number of therapeutic approaches have been developed to address tumour hypoxia, including reducing hypoxia by increasing oxygen availability, introducing chemical or physical sensitisation agents, or targeting radioresistant cells with higher radiation doses. Here, a theoretical tumour

control probability (TCP) analysis was performed to study the effects of reoxygenation where the dominant focal lesion, identified on pre-treatment T2-weighted magnetic resonance (MR) images, was modelled as a hypoxic subvolume. Material and Methods To model the effects of reoxygenation, the linear quadratic model was modified. The model split the prostate into two volumes, oxic and hypoxic. The oxic volume was defined as (PTV (prostate) - PTV (focal)), and the hypoxic volume was defined as focal PTV (focal). To simulate a hypoxic subvolume, the radiosensitivity parameters were reduced by a hypoxic reduction factor (HRF).

The equations above are the modified linear quadratic survival fractions for the oxic and hypoxic volumes. q is the HRF, α and β are the radiosensitivity parameters, numerical values of which were obtained from prostate cell line studies, and n is the number of fractions. A flux of hypoxic cells move into the oxic compartment between fractions due to reoxygenation. To account for the change in oxygen tension within the tumour volume with time, the reoxygenation rate was modified for each fraction. The number of surviving cells in each volume were added together following each fraction to get the total number of surviving cells N t , which was then used to calculate the TCP. Results Figure 1 shows the TCP model with different reoxygenation rates. The degree of reoxygenation determines how well the tumour responds to radiation, with larger reoxygenation rates giving improved tumour control at lower doses, which is observed in the following TCD 50 values, no-reox, 3% re-ox, 10% reox, 20% reox TCD 50 = 51.5, 49.9, 47.4, and 45.3 Gy respectively. Figure 1 : TCP model with varying reoxygenation.

Conclusion The prostate tumour response to radiation can be greatly improved by applying sufficient reoxygenation of the hypoxic subvolume. Future modelling could include different α and β values for the oxic and hypoxic volumes, since the hypoxic volume will be more radioresistant. Measuring hypoxia and identifying hypoxic subvolumes is an active area of research, incorporating them into TCP modelling will hopefully lead to better